Dr. Benjamin Bikman - 'Insulin vs. Glucagon: The relevance of dietary protein'

thanks Eric thanks for the introduction yeah I am an insulin mitochondria guy so what am i half of this conversation and insulin yes I can talk about glucagon will be the new character here before I get going though Jeff and rod thank you so much for the invitation I am delighted to be here again it's fun to be here now and see friendly faces as opposed to strangers like it was last year but last year was my first time when Jeff and rod reached out invited me that was my first step into the low carb community and it has just been delightful I have appreciated making new acquaintances and some genuine friendships and in fact as a scientist I've really appreciated some actual collaborations that are coming from me getting into this space so I am genuinely grateful thank you so today insulin versus glucagon I have been following conversations in the community with regards to the role of protein and it's been somewhat sometimes concerning when I hear the fear in people's voices and they talk about protein and so I've made that sort of an academic pursuit and decided to share with you some of my conclusions before I get going here's my disclosure I have two I'm a part of two groups insulin IQ where we are trying to make people more mindful of the relevance of insulin and health and the best my most favorite audiences are the Grand Rounds talks that I get to do to physicians and then best fats is just our efforts to contribute to this blossoming low carb high fat supplement space so last year of my first step into the low carb community I spoke about the relevance of insulin and ketones and the effects that they have on the contrasting effect on adipocyte mitochondrial uncoupling in other words white fat or brown fat I'm not going to talk about that today as you could tell from the title so collective disappointment I'm sure but let me give you an update so this was the paper we just published a few months ago my students and I published this paper in a good journal biochemical journal where we found that insulin basically as I talked about a year ago and we finished all the evidence here or put all the evidence in this paper insulin was I'm slamming on the brakes of mitochondrial uncoupling forcing the mitochondria in the fat tissue to be more tightly coupled in other words only use energy when you need it that's what insulin was doing I will give the final update next year we will have all the rest of the human data with regards to the ketones and I'll be able to tell the full story so if Jeff and rod haven't had enough of me then I'll see you next year same time same place okay now let's get into the story then so here's the pancreas in fact I had to pick this image for fear of using an image that looked a little dirty but I hopefully this is the pancreas tucked underneath the stomach and of all the myriad cells the pancreas has that cells that are involved in endocrine functions cells that are involved in digestive or exocrine functions we want to zoom in on the beta in the Alpha cells and these are famous because they produce insulin and glucagon respectively and then insulin and glucagon in addition what's interesting is that they're produced right beside each other in these little pockets of cells within the pancreas and yet they're enemies in a way and they're each antagonizing the other and almost every possible biochemical event if insulin is trying to do something glucagon is trying to stop it if glucagon is trying to do something insulin is trying to stop it so it's pretty much like my kids nevertheless we see insulin to quote Mike and Mary Danny needs because they said it well insulin is the hormone of feeding and storing and glucagon is the hormone of fasting and burning and what that means then in a bigger biochemical sense is that insulin is a hormone of anabolism or building things up taking simple molecules and making them into something bigger and keeping it and then glucagon wants to take the complex molecule and break it down usually breaking it down into an energy source that the body can then use so it is catabolic it is one of those fundamental or prototypical catabolic hormones whereas insulin is the prototypical anabolic now when we look at these hormones let's zoom in on what they're doing because now mind you insulin and glucagon are affecting most of the tissues of the body the insulin affects every cell of the body insofar as every cell has an insulin receptor and glucagon affects most but nevertheless let's look at these three very metabolically relevant tissues now you can't necessarily tell it I'm talking about here based on my pictures so we have muscle on the Left adipose tissue in the middle and then the liver on the far right when we look through each of these three tissues these hormones have varying effects in particular insulin is completely anabolic at the muscle promoting muscle synthesis and promoting like a Genesis or the storage of glucose in the muscle to be used later and glucagon has no effect this is one of those instances where there are no receptors for glucagon on muscle so glucagon has no catabolic actions it can't tell the muscle to do anything in contrast adipocytes have both receptors and so now we begin to see this antagonistic yin and yang between these two hormones insulin wants to promote the growth of the adipocyte by storing lipid through the PO Genesis glucagon wants to oppose that and induce the shrinking of the adipocyte through lipolysis or the breakdown of the stored lipid and then the antagonistic theme continues in the liver where insulin is telling the liver to make lipid and make glycogen or storing fat and storing on glucose loop a glucagon is antagonizing that we want to break down lipid we want to break down glucose we want to make glucose we also want to make ketones an alternative fuel if we can use that word or just another fuel for the body now they these hormones don't have comparable effects across these tissues so muscle is then completely driven by insulin in the case of just insulin and glucagon and then adipocytes appear to be more sensitive to insulin than they do to glucagon so if you had a one-to-one ratio of insulin to glucagon theoretically the insulin is going to win that tug-of-war insulin has the chokehold on the adipocyte in a similar way glucagon is the primary driver of whatever the liver is doing so if the livers sing both glucagon and insulin usually glucagon is going to be setting the tone it can beat insulin there as opposed to the adipocyte were insulin tends to win that race so just like these two hormones insulin and glucagon dictate the biochemical actions in these three metabolically relevant tissues and we could have listed more we need to explore how do then the macronutrients dictate the levels of insulin and glucagon and this isn't as clear as we usually think and this is this was the matter of my pursuing this topic it was to get to this issue when we look at carbohydrates we see this opposing effect where carbohydrates will in any situation increase insulin and reduce glucagon the textbook version is this complimentary effective protein where protein is both increasing insulin and glucagon making it somewhat of a macronutrient that people in low-carb community fear and and I'm not sure that's justified and I'm making the case that perhaps we need to revise the way we think about it and then fad and each of these are just when it's consumed in its pure form if you take a spoon of carb a spoon of protein or a spoon of fat fat will not increase insulin it will only increase glucagon and that makes it very friendly to those of us who appreciate or respect the relevance of insulin and the pathogenicity of insulin acknowledge that it has a hand in virtually every chronic disease now however one of these depends on context that when we've put these arrows the way the textbooks have and that's how I've done it it really depends on underlying glycemic status and it's insulin the insulin affect the insulin on genic affective protein is heavily influenced by the underlying glycemic status and other what we'll get into it in fact let's get into one study right here now by way of disclosure this is a study done in canines and but before you start thinking oh well that's not relevant to humans you actually will be hard-pressed to find a mammalian digestive system that is as similar to humans as canines even to the point of bacteria where canines have similar mouth and digestive bacteria as humans do so it is more relevant than you might think nevertheless challenge it as you will so in this study on the left hand side you'll see the only difference between these two instances is that on the left hand side they infused glucose and you'll see right along the very top it mentions a glucose infusion so they're providing these animals an underlying hyperglycemic state in the condition on the left it was there was no infusion and the animals were just simply in a fasted state and then they had those two repeated boluses of alanine infusions now alanine is relevant yes it's an amino acid in mind you of course once we ingest the protein it all gets broken down to amino acids so we always say well in protein spike my insulin we technically should say amino acids right but let nevertheless alanine is the why is it so relevant alanine is the prototypical gluconeogenic amino acid when we teach this concept how certain amino acids are gluco genic we use alanine as the textbook example because it's so good at bumping of glucose and you see that there you see that that green line takes a little skip up whenever they infuse the alanine now that's all interesting what happens then to the insulin and the glucose on on this left hand side what we see in the state were there there's an underlying elevated glucose level we see that insulin goes up massively 130 micro units per mil that is an incredible bump over where it was already elevated because of the hyperglycemia it went beyond that 130 more micro units so insulin responded remarkably to this amino acid infusion in contrast glucagon plummeted by almost half now when we compare this to the fasted animals look at that orange line insulin didn't change a bit and glucagon doubled isn't that a remarkable difference and the only difference is in one state there was elevated glucose in the other state there was not and the reason to explain this or how we explain this is we can't afford to inhibit gluconeogenesis because those animals were fasted if we had had a substantial insulin effect what would that have done to their fasting glucose levels and the animals would have lost consciousness so we can't afford to inhibit gluconeogenesis we need to keep that process going because that's the only way the animals are maintaining normal glycaemia because of that insulin was maintained and glucagon was elevated and we'll come back to this in a bit with some human data so with this somewhat revised system in place we will look at we I'm now showing what might be happening then with insulin and glucagon in the case of a low carb environment where there is not this consistent steady source or stream of carbohydrates spilling into the blood as glucose and then let's come back to these same three tissues so then in these instances now of the low carb individual consuming carbohydrate we still have the same effect of course in this case carbohydrate and protein are both anabolic at muscle and then fat would have no overt effect in this instance of the low-carb individual now mind you I say that carbon protein is anabolic that isn't to say that you can have muscle growth and not actually pay the price you know you can't just take a drink and say I'm getting big you got it you got to still earn it and then with the adipocyte carbohydrate once again is anabolic like it is everywhere in fact these two are similar because the adipocyte and the liver both contain insulin receptors and glucagon receptors we have this contrasting effect especially in the case of protein where there is going to be some degree of anabolic but also in the case of a low-carb individual a pronounced that we can't ignore catabolic effect where we're insulins trying to increase the storage and activate anabolic pathways glucagon is there to counter that especially in the low carb state and then to make this relevant or or to give it sort of a palatable easy takeaway i submit that one helpful way of looking at the relevance of all this is to consider the insulin - glucagon ratio and this is particularly relevant in the liver as we'll get into that in just a bit but the insulin glucagon ratio provides this underlying metabolic tone in other words it tells the body where the tissues the cells of the body is the prevailing metabolic pathway I need you to be undergoing or I need activated insulin glucagon ratio provides us some understanding of who's sort of winning in other words if it's a high insulin to glucagon ratio we know that anabolic pathways are predominating if in contrast it is a low insulin glucagon ratio then we know that the catabolic pathways are predominating and you know in this constant tug-of-war and all of this is always happening we have this constant check and balance but in these instances high insulin glucagon ratio represents an anabolic state low insulin and glucagon ratio represents a catabolic state now one thing that's noteworthy is almost sort of a pit stop before I go too much further having a low insulin the glucagon ratio is relevant because that is what I submit actually matters in a fasted State fasting has become very popular and perhaps there's some justification I sometimes worry a little bit about it people jumping on a little too quickly and maybe not fully informed of what's happening that there are some metabolic benefits but also some deleterious consequences but nevertheless there are benefits and I submit that most of the benefits occur due to this favorably low insulin and glucagon ratio because these this ratio induces these sorts of benefits where we see improvements in insulin sensitivity we see the activation of autophagy which is heavily driven by hormones insulin absolutely clamps down on a tofu Jie whereas glucagon activates it and we could say the same thing of this sort of sub process of etaf AG as known as my kava G where we are recycling old mitochondria keeping them healthy and viable and producing fewer reactive oxygen species then we have lipolysis predominating and then of course what I talked about last year we have the activation of brown adipose tissue all of these things are happening in this low insulin the glucagon ratio state that predominates a fasted State yet the benefit of a low carb diet in maintaining an a low insulin to glucagon ratio is that you get the benefits of this fasted state without actually starving the body your maintaining this fuel intake that allows the body to continue to function well and of course it can function well with fasting too but you're getting the benefits of fasting insofar as hormones are dictating most of the metabolic pathways we care about alright with that as the pitstop you can hopefully appreciate the benefits of a low insulin glucagon ratio let's look at what happens to insulin and glucagon when a person consumes three general dietary states the one is the standard American diet next would be just fasting in a fasted state and then the low carb diet and let's look at each of the insulin glucagon ratio in each of these three states so in a fasted state the insulin the glucagon ratio not surprising it's pretty low it's 0.8 that is a true sort of I say fasted I'm not talking 12 hours this is like a 24 plus hour sort of fast around point eight this is in humans we've left the canines behind so all the doubters skeptics come back this is absolutely an arguably a catabolic ratio of insulin to glucagon we have these catabolic processes activated and I'm saying that ketogenesis is catabolic someone would argue well it's anabolic it's catabolic but even still we've made a nutrient from it so I could appreciate the counter but it's a catabolic it's evidence of catabolism nevertheless we can all agree this insulin glucagon ratio of 0.8 must be catabolic because these are the catabolic processes that are active now in the case of someone consuming the standard American diet the insulin and glucagon ratio is quite high relatively at around for this we know is an anabolic state and we have the activation of anabolic processes like the storage of lipid the storage of glycogen and we have the inhibition of processes that a lot of us care about we're inhibiting autophagy and we are inhibiting ketogenesis we know that's happening in this fed state of the standard American diet with this insulin the glucagon ratio of around 4 now lastly our beloved low-carb diet here we have an insulin glucagon ratio of around 1.3 a little higher than the fasted state but substantially lower than the standard American diet fed State and once again we know in a low-carb diet where carbohydrate consumption is low or very low that is catabolic we have the same biochemical processes occurring in this low carb fed state as we do in the fasted state so we can say that just what we were seeing with the insulin glucagon ratio of 0.8 we're seeing generally the same processes activated at around 1.3 and I'm going to come back to this in the relevance of this number when we talk about the ingestion of protein but that brings me to that point what happens then when we add protein to the diet to these ratios we are a community that appreciates and respects insulin to what degree do we need to worry about the insulin genic effect of the amino acids as a part of the proteins that we ingest well let's look in the fasted State if someone is doing this long term issue fast hopefully they're being smart about it hopefully they're avoiding refeeding syndrome when they eat protein we see a change in the insulin glucagon ratio going from point 8 down to 0.5 and so we see this relative increase in glucagon over whatever relative change is happening with insulin that's not surprising that's exactly what we saw with the dogs do you remember how the insulin didn't change need the glucagon changed substantially it lowered the insulin the glucagon ratio so putting this person at least maintaining them in this very catabolic state now with the standard American diet are you ready when this person needs protein we see that their ratio goes up to 70 so about a 20 time increase and so this kind of gets to the heart this gets to the heart of our collective appreciation of the insulin of genic effects of the proteins we eat because it's justified but we have to put it in the right context for those of us who are controlling carbohydrates and have a healthy respect for insulin this this is us here now what do you think is going to happen you ready when a person eats protein on the low carb diet it changes from this relatively low level and goes up to there is in fact no change and technically speaking there's a 6% change which means that it stays at 1.3 there's a 6% change as opposed to this 20 times change that we saw in the standard American diet so if we put these two head-to-head and we feed them the diet's the standard American diet and the low-carb diet as was done years ago and we give them one gram per kilogram of protein and this is restored of recapping what we just talked about and we look at the insulin the glucagon effects we see that there is this dramatic increase in the insulin glucagon ratio on the standard American diet fed side and yet no such phenomenon occurring we have them mate the maintenance of the relatively low insulin glucagon ratio that we see with the standard American diet and so the numbers changed accordingly like we saw earlier the substantial effect and the standard American diet fed people who have glucose coming in quite readily the an insulin climbing into the protein simply adds to that it compounds the insulin effect of the carbohydrate where oral carbohydrate consumption is quite limited we see no such effect why might this be as a repeat in fact let me quote one of my heroes dr. Roger Unger he mentions without exception that the insulin the glucagon ratio is dictated by the need for gluconeogenesis and because in those low carb fed bodies gluconeogenesis is important it is important we can't afford to have insulin spiking too high because if it did it would clamp down on gluconeogenesis and the person would become hypoglycemic now let's look at the liver and look at this particular process in just a little more detail in the standard American diet and the low carb diet I'm I'm submitting to you that the reason we have these differences in the insulin glucagon ratio is because of the need for gluconeogenesis in the standard American diet state there is no need for gluconeogenesis in the low carb fed state we need gluconeogenesis and I'm saying that and yet even as I'm saying we need the glucose as a scientist I only know of one cell that actually glucose and we know there's no exception do you wanna do you wanna do you know what it is some people are saying brain and yet I've never seen a study that proves has any one I'm putting this out there the beta cell kit you can't use any other fuel neither ketone or liquid or anything else it can it can I think so but it's erythrocytes we know erythrocytes we know for a fact that's my little erythrocyte there we know for a fact erythrocytes that lack any sort of mitochondrial presence absolutely must use glucose for feel there's an alternative we always say that brain needs glucose and yet well the brain readily uses ketones in fact I would submit the brain prefers ketones because as ketones become available the brain begins using it more and displaces the glucose but I appreciate this as purely academic because you couldn't test this in a living mammal because they would die from the lack of glucose but there's no study that I have ever seen that proves the brain needs glucose can you see where I'm going I've never seen that being proved but that's way off topic but maybe someone will talk about that later anyway if you know if anyone knows of a study that proves that I genuinely would love to know okay so we have gluconeogenesis we have these respective insulin glucagon ratios high insulin to glucagon ratio and the sad low insulin the glucagon ratio in the in the low carb and in each instance we have this very expected regulation of gluconeogenesis where we have the inhibition of gluconeogenesis in the high ratio state and the activation of gluconeogenesis in the low insulin glucagon ratio state now in addition to regulating gluconeogenesis what else do insulin and glucagon regulate at the liver what do you think ketogenesis yeah this beloved process or feared or much maligned whoever we're talking with but nevertheless they both regulate ketogenesis just like they regulate gluconeogenesis and here the standard American diet and it's roughly insulin glucagon ratio of four very potently inhibits the insulin to inhibits ketogenesis sorry and then the low insulin of glucagon ratio the low-carb diet activates ketogenesis now then what is the relevance of protein in this process and this is why many people fear protein because they're chasing their ketones so doggedly that they worry wolf it's gonna kick me out of ketosis I can't eat it and I I submit and the reason I wanted to talk about this is that I think that leads to somewhat bizarre eating in a way where we we end up issuing real food because I has protein in it and we end up just adding oil to everything and I I'm not I don't think that's the best way to do it even if it if there is some alteration in ketosis nevertheless let's briefly just look at the biochemical process of how ketogenesis occurs yes indeed low insulin is in fact a part in fact a necessary part of ketogenesis but the other part of this is that we must have elevated glucagon and this was highlighted in the study published just last year by some very good friends of mine and you'll see along the y-axis they're measuring this relative change in beta hydroxy butyrate in these animals and along the bottom it's a somewhat confusing axis in a way so I'm going to clarify it they had animals with functioning beta cells producing insulin in animals that were not producing insulin then they had within that those groups subgroups of animals with functioning glucagon receptors at the liver in animals without functioning glucagon receptors and in other words no glucagon signaling and then let's look first then at the no glucagon States between insulin and no insulin within that group we see that in the absolute absence of insulin we see ketones go up from the left side to the right side by about four or so times a small little bump right and if you think about insulin being the absolute driver of ketogenesis you'd think if there is no insulin which there's none in those animals that we're talking about an untreated type one diabetic here you would say well they're dying from ketoacidosis there should be massive amounts of of Keith Keith of ketones here there should be well into ketoacidosis and yet there's just a very subtle increase that we would say that there may be in ketosis in this state that's because there's no there are no functioning glucagon receptors when we then look at the differences but insulin deficiency or surplus and functioning glucagon signaling we see that once we add glucagon signaling into the mix we have this almost 50 times increase in ketone production and this is just simply indicative of the need for functioning glucagon in the process of ketogenesis and the fact that Kia protein increases glucagon then is another reason to appreciate the protein and indeed even the proteins ketogenic effect and this was highlighted by one of my other academic heroes Denis McGarry where he mentions that glucagon is the primary driver of ketogenesis in the liver but despite me emphasizing insulin and glucagon before I finished this little bit let me mention that there is one other player that needs to be discussed and that is carnitine and this fact this was mentioned earlier I think Rob Wolfe mentioned this yesterday carnitine is this escort basically not in a bad way it is escorting it is escorting the lipid into the mitochondria allowing the lipid to be oxidized and just as a reminder we must have a lipid be oxidized for it to then be ketogenic we have to get down cleaving off those pieces those two little pieces of carbons at a time and then that B kid that turns into acetyl co a and then that gets turned into the ketone that we know and love so we have to have sufficient carnitine to escort the lipid into the mitochondria and induce the oxidation and then we have the magic of ketogenesis so all of these are relevant this was a study by Denis McGarry in animals and rodents where he took the the livers out of animals that were fed and fasted and you see that when the animals were fasted the level of ketones was about three times higher that's that upper level and in the fed animals he simply took and fed their normal standard Chow and then supplemented carnitine now mind you we all make carnitine but there are in fact known instances of carnitine deficiencies where the human is enabled to create sufficient carnitine for functional medic Andreea processes so in this state they added carnitine to these animals and look it would happen to ketogenesis so I'm simply wanting us to appreciate there's this extra player here where we need sufficient carnitine for ketogenesis well indeed we need it for just lipid oxidation in any general sense so these are the three characters then or or pout the parts or components of the formula where we look we need a low insulin level an elevated glucagon level and at least sufficient carnitine and then we've created we have the formula for ketones now this is a pretty academic way of looking at it me saying low insulin increased glucagon and perhaps the more practical side is to simply add in the relevant macronutrients and I submit when we're eating a real diet and nevertheless appreciating the relevance of carbohydrates and keeping them controlled it ends up being a mix that would look something like this where we have protein combined with fat combined with carnitine providing the recipe for ketogenesis and you might look at this and say well where could we get such a magical food that contains it's this wonderful mix of stuff well it's not very hard to find it red meat is the perfect source of these three components of ketogenesis now I appreciate as I as I have been offering this version of a low-carb diet that is not a shewing protein to the degree that some people do I appreciate that I may be inadvertently upsetting people and so here's my diplomatic conclusion here there are multiple ways of course to do what to adhere to a low-carb diet I kind of have two versions of that presented here on the left it's a version that is somewhat more appreciative of protein on the right it's a version that is wary of protein but what do they have in common they both are controlling carbohydrates and that really is the common strength between these two and that's that's the foundation that they share and then what might be relevant in determining which of these two versions of the low-carb diet is best I submit perhaps it's helpful to consider the underlying glycemic status of the individual in other words if someone is starting from this metabolically unhealthy state of hyperglycemia and hyperinsulinemia in other words pre-diabetes up to type-2 diabetes most of most of the adults in the civilized world or industrial and not even industrialized we have this very common it there may be justification to be a little wary of protein at first perhaps depending on what the person would prefer to eat nevertheless I submit the unifying sort of version of these two or hypothesis or union of these two versions of the low-carb diet could be that the person is starting in this version on the right where it is relatively low in protein and then they're progressing as the insulin and glycemia is improving towards this state that is still controlling carbohydrates yet acknowledging the relevance of protein now then what might this look like because I'm not your physician I'm gonna give you some advice and I have no fear of litigation because this is purely academic here's mine here's one way you might do this and this is my sort of cheeky attempt at making it memorable and and of course I'm using alliteration quite heavily so firstly I submit to maintain a low insulin the glucagon ratio a person one must control carbohydrates to a person then I submit would be well-served by then prioritizing protein ensuring sufficient protein intake to maintain lean body mass and healthy function and then third all the remaining calories are filled with fat and so let's talk about each of these with just a moment in more detail very briefly by controlling carbohydrates I do mean this very widely accepted range of around 50 grams or so per day and this depends of course on the person and that would have to be optimized a little lower or a little higher whether the person can fudge it up a little bit but nevertheless whatever range they come to to have a healthy range for that person they do need to scrutinize the quality of the carbohydrate and this is no surprise of course I exclusively define a carbohydrate as good or bad based on the degree to which it's going to spike insulin and so this would be just some very simplistic version of that next one prioritized protein by this I mean that when a person is ensuring I'm sufficiently controlled carbohydrate consumption there is then I submit a benefit to ensuring the person's getting that range of protein one to two grams per kilogram body weight and please throughout this talk I've had references in coroner's if I ever feared there was something deeply controversial please look into this and make your own conclusions just like I've done by just pursuing data and coming to a conclusion but I submit to you to maintain healthy lean body mass we need to be make sure we're getting in that range and I think our love of fat sometimes prevents us from getting that and that's why I wanted to mention this now mind you as I just turned 40 very recently a mindful of my getting older and my kids are getting older they're our need for dietary protein goes up as we age so as we're getting older we need to make sure we're on the higher end dr. Stuart Phillips has found that and he's really one of the legends in this area that the older we get the less capable our body is at converting ingested protein into muscle protein so we do indeed need a little more and I worry that we're sometimes not getting it and then third as I mentioned we fill all the remaining calories whether that's 1,500 or 2,000 calories that is fat all of our remaining caloric needs come from fat and once again as our we know this very well and nina spoke about this very well yesterday we need to scrutinize the quality and in essence i basically say we just stick with the fats we've been eating as a species since time immemorial it was either eat it from the animal or make a Leever big enough to compress the fruit and get the oil from the fruit it was simple we've been doing it so animal and fruit fats I submit are better than any industrial seed oils as we all know and so in some I submit that this overly simplistic paradigm of three steps of a healthy diet it is I consider healthy because it maintains what I consider a smart metabolically prudent insulin the glucagon ratio keeping it low keeping it in control allowing the benefits of the fasted state yet without the need for caloric restriction and then it also ensures that we are properly nourishing the body we're giving the body what it needs by making sure that there's some focus on protein or to maintain the alliteration a priority on protein with that I thank you for listening and I look forward to any questions during the Q&A thank you [Applause]

Channel: Low Carb Down Under

Views: 435,862

Rating: 4.9251785 out of 5

Keywords: Low Carb Down Under, www.lowcarbdownunder.com.au, LCDU, Low Carb Breckenridge 2018, #LowCarbBreck, #LCB18, Ben Bikman, LCHF, Low Carb High Fat, Carbohydrate Restriction, ketogenic diet, insulin, developmental biology, physiology, InsulinIQ, best fats

Id: z3fO5aTD6JU

Length: 36min 0sec (2160 seconds)

Published: Sun Apr 08 2018

Reddit Comments

[u/JudgesWillAcceptIt]

Not at a place to watch the video. I know Dom D'agostino who studies it quite thoroughly says it can kick you our if ketosis.

Isn't it just a simple blood test test to see if it kicks you out?

Why is there a debate?

Once again, I'm not able to watch it. I have it saved.

[u/krpcannon]

I started keto over a year ago now. I wasted a year of my life - eating under 100g (I weigh 140lb) of protein lead to persistently low energy and horrible athletic performance. The importance of eating a reasonable amount of protein is over-emphasized heavily. Also - has anyone notice that increasing protein improves cognition?

[u/[deleted]]

Great video

[u/jmor88]

Good to hear, I figured that eating too much protein would not spike insulin or kick me out of ketosis.

[u/soldier123456]

Summary:

Protein is the fucking shit. Do not be scared of it.

Protein does not spike insulin if you are on keto. In contrast if you eat a normal American diet, protein spikes insulin.

Red meat contains carnitine which is key for ketosis, so do not be scared of red meats.

Consume more Protein, less than 50g from low glycemic carbs, and the rest fats.

Protein does not affect ketosis.

[u/BloodAtreyu]

Can someone summarize it, currently at work and really interested in it

[u/alexdevero]

If anyone still wants to ask if too much protein will kick him out of ketosis, watch this video.